To characterize the endothelial cell surface membrane glycoproteins that mediate thrombin stimulation of PGI2 synthesis by human umbilical vein endothelial cells (HUVEC), HUVEC were stimulated with thrombin in the presence or absence of different lectins. Of the lectins tested, only wheat germ agglu
Cytosolic calcium rises and related events in ergosterol-treated Nicotiana cells
β Scribed by Parul Vatsa; Annick Chiltz; Estelle Luini; Elodie Vandelle; Alain Pugin; Gabriel Roblin
- Publisher
- Elsevier Science
- Year
- 2011
- Tongue
- English
- Weight
- 821 KB
- Volume
- 49
- Category
- Article
- ISSN
- 0981-9428
No coin nor oath required. For personal study only.
β¦ Synopsis
The typical fungal membrane component ergosterol was previously shown to trigger defence responses and protect plants against pathogens. Most of the elicitors mobilize the second messenger calcium, to trigger plant defences. We checked the involvement of calcium in response to ergosterol using Nicotiana plumbaginifolia and Nicotiana tabacum cv Xanthi cells expressing apoaequorin in the cytosol. First, it was verified if ergosterol was efficient in these cells inducing modifications of proton fluxes and increased expression of defence-related genes. Then, it was shown that ergosterol induced a rapid and transient biphasic increase of free CaΒ²βΊ which intensity depends on ergosterol concentration in the range 0.002-10 ΞΌM. Among sterols, this calcium mobilization was specific for ergosterol and, ergosterol-induced pH and CaΒ²βΊ changes were specifically desensitized after two subsequent applications of ergosterol. Specific modulators allowed elucidating some events in the signalling pathway triggered by ergosterol. The action of BAPTA, LaClβ, nifedipine, verapamil, neomycin, U73122 and ruthenium red suggested that the first phase was linked to calcium influx from external medium which subsequently triggered the second phase linked to calcium release from internal stores. The calcium influx and the CaΒ²βΊ increase depended on upstream protein phosphorylation. The extracellular alkalinization and ROS production depended on calcium influx but, the ergosterol-induced MAPK activation was calcium-independent. ROS were not involved in cytosolic calcium rise as described in other models, indicating that ROS do not systematically participate in the amplification of calcium signalling. Interestingly, ergosterol-induced ROS production is not linked to cell death and ergosterol does not induce any calcium elevation in the nucleus.
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